BASIS FOR DEFECTIVE PROLIFERATION OF PERIPHERAL-BLOOD T-CELLS TO ANTI-CD2 ANTIBODIES IN PRIMARY SJOGRENS-SYNDROME

Anti-CD2-induced T cell proliferation was analyzed in the peripheral blood samples of 31 primary and 8 secondary untreated Sjogren's syndrome patients. Anti-CD2-stimulated PBMC proliferation was very low in about one-third of primary Sjogren's syndrome samples, despite the number of CD2+ cells being similar in primary and secondary Sjogren's syndrome and normal PBMC samples. The depressed response to anti-CD2 was mainly found in anti-Ro+/La+ patients. Experiments on purified T cells demonstrated that a defect at the T cell level was responsible for the anti-CD2 unresponsiveness. Cell proliferation failure was associated with poor IL-2 and IL-2 receptor mRNA expression and, consequently, IL-2 and IL-2 receptor synthesis. Since defective anti-CD2-induced mitogenesis could be reversed by phorbol myristate acetate, but not calcium ionophore A23187, it is probably correlation with impaired protein kinase C activation. Comparison of anti-CD2-triggered PBMC proliferation in treated and untreated patients and a long-term study of nine patients showed that the defect is a stable characteristic in primary Sjogren's syndrome patients, but that it can be reversed by pharmacological immunosuppression.